scholarly journals Characterization of the Cardiovascular Responses to Intrathecal Administration of Angiotensin II (Ang II) in Conscious Rats

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Britta Veitenheimer ◽  
John Osborn
Keyword(s):  
Angiotensin Ii ◽  
Cardiovascular Responses ◽  
Intrathecal Administration ◽  
Ang Ii ◽  
Conscious Rats

Cardiovascular responses to intrathecal vasopressin in conscious and anesthesized rats

1989 ◽  
Vol 256 (1) ◽  
pp. R193-R200 ◽  
Author(s):  
A. Martinez-Arizala ◽  
J. W. Holaday ◽  
J. B. Long
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Intrathecal Administration ◽  
Motor Dysfunction ◽  
Sprague Dawley ◽  
Cardiovascular Changes ◽  
Conscious Rats

Increases in mean arterial pressure and heart rate have been documented after the intrathecal administration of [Arg8]vasopressin (AVP) in rats. Prior studies in our laboratories with conscious rats indicated that these cardiovascular changes were associated with a marked hindlimb sensorimotor dysfunction. In this study, which represents the first systematic comparison of the effects of intrathecal AVP in conscious and anesthesized rats, we demonstrate that in conscious male Sprague-Dawley rats 1) the motor dysfunction induced by intrathecal AVP is accompanied by a rise in mean arterial pressure that is significantly greater than that produced by an equal intravenous dose of AVP, and 2) both paralytic and pressor effects of intrathecal but not intravenous AVP are blocked by the intrathecal administration of the V1-receptor antagonist d(CH2)5[Tyr(Me)2]AVP (V1-ANT) but are not blocked by intravenous phenoxybenzamine, hexamethonium, or [Sar1, Thr8]angiotensin II, an angiotensin II antagonist. In contrast, in anesthesized rats the arterial pressor response to intrathecal AVP was blocked by intrathecal V1-ANT, intravenous hexamethonium, and intravenous phenoxybenzamine. Furthermore, conscious but not anesthesized rats exhibited a tachyphylaxis to intrathecal AVP. These results indicate that intrathecal AVP produces both the cardiovascular changes and the sensorimotor deficits through interactions with centrally located V1-receptors. In addition, sympathetic catecholaminergic mechanisms mediate the rise in mean arterial pressure produced by intrathecal AVP in anesthesized rats, but they do not in conscious rats.

Median preoptic nucleus ablation does not affect angiotensin II-induced hypertension

1986 ◽  
Vol 251 (1) ◽  
pp. H148-H152
Author(s):  
G. D. Fink ◽  
C. A. Bruner ◽  
M. L. Mangiapane
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Base Line ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Water Excretion ◽  
Median Preoptic Nucleus ◽  
Induced Hypertension

Previous studies implicated the ventral median preoptic nucleus (MNPOv) in cardiovascular responses to circulating and intracerebroventricular angiotensin II (ANG II) and in normal cardiovascular and fluid homoeostasis. In the present experiments, chronically catheterized rats received continuous (24 h/day) intravenous infusions of ANG II (10 ng/min) for 5 days, and changes in mean arterial pressure, heart rate, water intake and urinary electrolyte and water excretion were determined daily. Three groups of rats were compared as follows: 1) sham-operated control rats (n = 12), 2) rats with 20-70% of the MNPOv ablated electrolytically (n = 6), and 3) rats with over 90% of the MNPOv ablated (n = 5). The organum vasculosum of the lamina terminalis was intact in all three groups. Base-line values of all measured variables were identical in the three groups on two control days preceding ANG II infusion and on two recovery days after infusion. During the administration of ANG II for 5 days, mean arterial pressure rose significantly (and similarly) in all three groups of rats; no other variable was significantly affected by ANG II infusion. These results suggest that neural pathways originating in, or passing through, the MNPOv region are not critical in the pathogenesis of ANG II-induced hypertension in the rat.

Plasma vasopressin response to peripheral administration of angiotensin in conscious rats

1985 ◽  
Vol 248 (2) ◽  
pp. R249-R256 ◽  
Author(s):  
K. Yamaguchi ◽  
M. Koike ◽  
H. Hama
Keyword(s):  
Angiotensin Ii ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Mannitol Solution ◽  
Injection Volume ◽  
Conscious Rats ◽  
Plasma Vasopressin ◽  
Series Of Experiments

To assess a role for peripherally administered angiotensin II (ANG II) in regulating vasopressin (antidiuretic hormone, ADH) release, the effects on plasma ANG II and ADH of intraperitoneal injections of ANG II dissolved in various solutions were examined in conscious rats. Plasma ANG II and ADH were determined by radioimmunoassay using the trunk blood collected after decapitation. Injections of 150 mM NaCl containing ANG II (6, 12, or 24 micrograms X 2 ml-1 X 100 g body wt-1) caused dose-related increases in plasma ANG II 15 and 30 min after, but plasma ADH remained unchanged. The lack of effect on plasma ADH of the ANG II dissolved in isotonic saline was also confirmed in another series of experiments in which the solution with a higher ANG II concentration was loaded by much smaller injection volume (14.3 micrograms X 0.1 ml-1 X 100 g-1). However, when given together with 600 mM NaCl, ANG II (8 micrograms X 2 ml-1 X 100 g-1) significantly potentiated the plasma ADH response to the vehicle at 15, 30, and 60 min, without affecting those of plasma osmolality, sodium, and hematocrit. The elevations of plasma ANG II and osmolality brought about by the treatment were comparable with those previously observed in rats deprived of water for 46 h. ANG II was without effect on the plasma ADH responses to the intraperitoneal injections of hypertonic sucrose or mannitol solution that did not alter plasma sodium, although these solutions were equipotent to 600 mM NaCl in augmenting plasma ADH and osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

Contrasting Cardiovascular Responses from Intrathecal Administration of Epinephrine and Norepinephrine in Conscious Rats

1992 ◽  
Vol 20 (3) ◽  
pp. 367-374 ◽  
Author(s):  
Kathryn Gradin ◽  
Anthony P. Nicholas ◽  
Paul Hjemdahl ◽  
Torgny Svensson ◽  
Tomas Hökfelt
Keyword(s):  
Cardiovascular Responses ◽  
Intrathecal Administration ◽  
Conscious Rats

Respiratory effects of pressor and depressor agents in conscious rats

1998 ◽  
Vol 76 (7-8) ◽  
pp. 707-714 ◽  
Author(s):  
Julia KL Walker ◽  
Donald B Jennings
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Arginine Vasopressin ◽  
Bolus Injection ◽  
Ang Ii ◽  
Conscious Rats ◽  
Pressure Threshold ◽  
Pressure Changes ◽  
Pressor Agent

We hypothesized that the respiratory baroreflex in conscious rats is either more transient, or has a higher pressure threshold than in other species. To characterize the effect of arterial pressure changes on respiration in conscious rats, ventilation (V) was measured by the plethysmographic technique during injections, or infusions, of pressor and depressor agents. Bolus injections of angiotensin II (Ang II) or arginine vasopressin (AVP), transiently increased mean arterial pressure (MAP; mean ± SE) 43 ± 6 and 28 ± 5 mmHg (1 mmHg = 133.3 Pa), respectively, and immediately reduced tidal volume (Vt) and, in the case of AVP, V. In contrast, by 10 min of a sustained elevation of MAP (40 ± 3 mmHg) with infusion of Ang II, Vt, f, and V were not different from control levels. Bolus injection of sodium nitroprusside (SNP) to lower MAP (-28 ± 3 mmHg) immediately increased breathing frequency (f) and V, whereas sustained infusion of SNP to lower MAP (-21 ± 3 mmHg) did not change f or V at 10 and 20 min. In conscious rats, both injection and infusion of the pressor agent PE (+40 to 50 mmHg) stimulated f and V; this contrasted with anesthetized rats where PE inhibited f and V, as reported by others. In conscious rats, respiratory responses associated with baroreflexes adapt rapidly and, in the case of PE, can be overridden by some other mechanism.Key words: angiotensin II, arginine vasopressin, baroreceptor reflex, phenylephrine, sodium nitroprusside.

Baroreceptor denervation profoundly enhances cardiovascular responses to central angiotensin II

1989 ◽  
Vol 257 (1) ◽  
pp. H314-H323 ◽  
Author(s):  
K. W. Barron ◽  
A. J. Trapani ◽  
F. J. Gordon ◽  
M. J. Brody
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Rapid Onset ◽  
Inhibitory Effect ◽  
Ang Ii ◽  
Conscious Rat ◽  
Reflex Arc ◽  
Circulatory Control ◽  
Increased Sensitivity

The purpose of this study was to examine the influence of arterial baroreflexes on the pressor and regional hemodynamic responses to centrally administered angiotensin II (ANG II) in the conscious rat. Fourteen days after sinoaortic baroreceptor denervation (SAD) or the equivalent sham surgery, the pressor and hindquarters vascular resistance responses to intravenous administration of ANG II were augmented in the SAD group. The pressor and vasoconstrictor responses to intracerebroventricular ANG II were also augmented after SAD; however, the SAD animals were more than 1,000-fold more sensitive than the sham group to the pressor effects of intracerebroventricular ANG II. Further experiments demonstrated that 1) the enhanced pressor response to intracerebroventricular ANG II in the baroreceptor-denervated group was due to similar increases in sympathetic outflow and vasopressin mediated vasoconstriction, 2) the increased sensitivity to central ANG II occurs as soon as 1 h after SAD, and 3) the enhanced pressor effects to intracerebroventricular ANG II also occur with intracerebroventricular hypertonic saline. We conclude that arterial baroreflexes exert a potent central inhibitory effect on the central pressor actions of ANG II that are greater than can be accounted for by the peripheral reflex arc. Finally, because of the rapid onset of the increased responsiveness to central ANG II after SAD, we propose that baroreflex buffering of central pressor stimuli may be tonically involved in circulatory control.

NO and endogenous angiotensin II interact in the generation of renal sympathetic nerve activity in conscious rats

2004 ◽  
Vol 286 (4) ◽  
pp. H1258-H1265 ◽  
Author(s):  
Donogh F. McKeogh ◽  
Theresa L. O'Donaughy ◽  
Virginia L. Brooks
Keyword(s):  
Angiotensin Ii ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Rats ◽  
Renal Sympathetic Nerve ◽  
Low Sodium ◽  
Renal Sympathetic

Nitric oxide (NO) appears to inhibit sympathetic tone in anesthetized rats. However, whether NO tonically inhibits sympathetic outflow, or whether endogenous angiotensin II (ANG II) promotes NO-mediated sympathoinhibition in conscious rats is unknown. To address these questions, we determined the effects of NO synthase (NOS) inhibition on renal sympathetic nerve activity (RSNA) and heart rate (HR) in conscious, unrestrained rats on normal (NS), high-(HS), and low-sodium (LS) diets, in the presence and absence of an ANG II receptor antagonist (AIIRA). When arterial pressure was kept at baseline with intravenous hydralazine, NOS inhibition with l-NAME (10 mg/kg iv) resulted in a profound decline in RSNA, to 42 ± 11% of control ( P < 0.01), in NS animals. This effect was not sustained, and RSNA returned to control levels by 45 min postinfusion. l-NAME also caused bradycardia, from 432 ± 23 to 372 ± 11 beats/min postinfusion ( P < 0.01), an effect, which, in contrast, was sustained 60 min postdrug. The effects of NOS inhibition on RSNA and HR did not differ between NS, HS, and LS rats. However, when LS and HS rats were pretreated with AIIRA, the initial decrease in RSNA after l-NAME infusion was absent in the LS rats, while the response in the HS group was unchanged by AIIRA. These findings indicate that, in contrast to our hypotheses, NOS activity provides a stimulatory input to RSNA in conscious rats, and that in LS animals, but not HS animals, this sympathoexcitatory effect of NO is dependent on the action of endogenous ANG II.

Spinal angiotensin II influences reflex cardiovascular responses to muscle contraction

1995 ◽  
Vol 269 (4) ◽  
pp. R864-R868 ◽  
Author(s):  
C. L. Stebbins ◽  
S. Bonigut
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Angiotensin Ii ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Ang Ii ◽  
Exercise Pressor Reflex ◽  
Static Contraction ◽  
Pressor Reflex

We tested the hypothesis that inhibition of angiotensin II (ANG II) AT1 receptors in the thoracic spinal cord attenuates the reflex cardiovascular response to electrically induced hindlimb static contraction (exercise pressor reflex). Consequently, in alpha-chloralose-anesthetized cats, contraction-induced increases in mean arterial blood pressure, maximal rate of rise in left ventricular pressure (dP/dt), and heart rate were compared before and after intrathecal injection of the AT1 receptor antagonist losartan (100 or 1,000 micrograms; n = 7). Losartan significantly diminished increases in blood pressure and maximal dP/dt provoked by static contraction by 33 +/- 5 and 31 +/- 6%, respectively. Conversely, these contraction-induced responses were unaffected by similar injection of ANG II into the lumbosacral spinal cord (n = 5). Moreover, intravenous injection of 100 micrograms losartan did not affect the cardiovascular response to contraction. Our data suggest that ANG II has a excitatory effect on the efferent arm of the exercise pressor reflex, which may be due to a facilitatory action on sympathetic nerve activity.

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